Exhibit 99.1

DeFi: A Phase 3 Trial of Nirogacestat for Progressing Desmoid Tumors (DT) Bernd Kasper , Ravin Ratan, Thierry Alcindor, Patrick Schöffski, Winette T. van der Graaf, Breelyn A. Wilky, Richard F. Riedel, Allison Lim, L. Mary Smith, Stephanie Moody, Steven Attia, Sant Chawla, Gina D’Amato, Noah Federman, Priscilla Merriam, Brian A. Van Tine, Bruno Vincenzi, Shivaani Kummar, Mrinal Gounder, on behalf of the DeFi Study Investigators ​ September 10, 2022

Content of this presentation is copyright and responsibility of the author. Permission is required for re - use . Declaration of Interests ▪ Bernd Kasper’s declaration of interests : ▪ Financial interests ▪ Ayala (advisory board, personal), Bayer (advisory board, personal), Blueprint, (advisory board, personal), Boehringer Ingelheim (advisory board, personal), GSK (advisory board, personal), PharmaMar (advisory board, personal), SpringWorks Therapeutics (advisory board, personal) ▪ Nonfinancial interests ▪ Ayala (coordinating PI, institutional, no financial interest), PharmaMar (coordinating PI, institutional, no financial interest), SpringWorks Therapeutics (coordinating PI, institutional, no financial interest), European Organisation for Research and Treatment of Cancer (EORTC ; leadership role, Chair of the EORTC Soft Tissue and Bone Sarcoma Group [STBSG]) Kasper et al. DeFi Phase 3 in Adult Desmoid Tumors

Content of this presentation is copyright and responsibility of the author. Permission is required for re - use . Gamma Secretase Inhibition in Desmoid Tumors ▪ Desmoid tumors (DT) are rare, locally aggressive, and invasive soft - tissue tumors that are challenging to manage due to variable presentation, unpredictable disease course, and a lack of approved therapies 1,2 ▪ Treatment should be individualized to optimize tumor control and improve symptom burden, including pain, physical function, and overall quality of life 3 – A global consensus initiative has been launched by The Desmoid Tumor Working Group aiming to harmonize management strategies 4 ▪ There is mechanistic rationale for the use of gamma secretase inhibitors (GSI) in DT as these tumors highly express Notch, which can be blocked by GSIs 5,6 ▪ Nirogacestat is an investigational, oral, selective, small - molecule GSI that has shown evidence of antitumor activity in DT in Phase 1 and 2 trials with a manageable adverse event profile 1,7,8 Image adapted from Andersson et al. Development (2011) and Bui and Kummar. Oncotarget (2017). Wnt pathway Notch pathway Notch Extracellular Plasma membrane Intracellular DvI Axin GSK3 APC - catenin HES1 Tcf4 Crosstalk Canonical Wnt signaling NICD Wnt DT, desmoid tumor; GSI, gamma secretase inhibitor; NICD, Notch intracellular domain. 1. Villalobos et al. Ann Surg Oncol. 2018;25:768 - 775. 2. Kasper et al. Oncologist. 2011;16:682 - 693. 3. Gounder et al. Cancer. 2020;126:531 - 539. 4. Desmoid Tumor Working Group. Eur J Cancer. 2020;127:96 - 107. 5. Andersson et al. Development. 2011;138:3593 - 3612. 6. Gounder et al. Cancer. 2015;121:3933 - 3937. 7. Messersmith et al. Clin Cancer Res. 2015;21:60 - 67. 8. Kummar et al. J Clin Oncol. 2017;35:1561 - 1569. Kasper et al. DeFi Phase 3 in Adult Desmoid Tumors

Content of this presentation is copyright and responsibility of the author. Permission is required for re - use . Nirogacestat 150 mg BID Placebo BID ▪ Histologically confirmed DT with progressive disease per RECIST v1.1 a ▪ Treatment - naïve with DT not amenable to surgery, or ▪ Refractory or recurrent disease (after ≥1 line of therapy) Adult Eligible Patients Radiographic p rogressive disease d Open - label nirogacestat 150 mg BID ▪ Global, randomized, double - blind, placebo - controlled, Phase 3 trial comparing the efficacy, safety, and tolerability of nirogacestat vs placebo in adult patients with progressing DT ▪ 142 patients randomized across 37 sites in North America and Europe ▪ Primary: Progression - free survival b ▪ Secondary: Objective response rate and patient - reported outcomes, such as pain, symptom burden, physical/role function, and overall quality of life c Trial Summary Key Endpoints Randomized 1:1 Stratified by tumor location (intra - vs extra - abdominal) 28 - day cycles DeFi: Phase 3 Study of Nirogacestat vs Placebo in Adult Patients With DT a Progressive disease defined by histologically confirmed DT that has progressed ≥20% within the past 12 months by RECIST v1.1. Ta rget tumors identified at screening by the Investigator. b Progression was determined radiographically using RECIST v1.1 or clinically by independent, blinded, central radiologic or cl ini cal review. c As assessed by change from baseline for BPI - SF, GODDESS DTSS, GODDESS DTIS, and EORTC QLQ - C30 at Cycle 10. d Radiographic disease progression or once the required number of events have been observed and the primary progression - free survi val analysis has been completed. BID, twice - daily dosing; BPI - SF, Brief Pain Inventory – Short Form; DT, desmoid tumor; DTIS, GODDESS DT Impact Scale; DTSS, GODDES S DT Symptom Scale; EORTC QLQ - C30, European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire - Core 30; GODDESS, GOunder/Desmoid Tumor Research Foundation DEsmoid Symptom/Impact Scale; RECIST, Response Ev aluation Criteria in Solid Tumors. ClinicalTrials.gov. https://clinicaltrials.gov/ct2/show/NCT03785964. Accessed August 24, 2022. Kasper et al. DeFi Phase 3 in Adult Desmoid Tumors Primary Analysis Data Cutoff: April 7, 2022

Content of this presentation is copyright and responsibility of the author. Permission is required for re - use . Baseline Demographics and Characteristics a Evaluable samples not available for all patients. Samples were analyzed for 51 and 53 patients in the nirogacestat and placeb o a rms, respectively. b Defined as a score of >4 calculated as the average of the daily BPI – SF Item 3 “Worst Pain in Past 24 hours” over the 7 - day perio d before the baseline visit. API, average pain index; BPI - SF, Brief Pain Inventory – Short Form ITT; intention to treat. Demographics/Characteristics, ITT Population Nirogacestat (n=70) Placebo (n=72) Age, median (range), y 33.5 (18, 73) 34.5 (18, 76) Sex, n (%) Male Female 25 (36) 45 (64) 25 (35) 47 (65) Somatic mutations in analyzed patients, n (%) a APC CTNNB1 11 (22) 43 (84) 11 (21) 42 (79) Tumor location, n (%) Intra - abdominal Extra - abdominal 17 (24) 53 (76) 18 (25) 54 (75) Focal category, n (%) Single Multifocal 43 (61) 27 (39) 41 (57) 31 (43) Desmoid tumor treatment status, n (%) Treatment naïve Refractory/Recurrent 18 (26) 52 (74) 14 (19) 58 (81) Number of lines of any prior therapy, median (range) 2 (0, 14) 2 (0, 19) Prior therapies, n (%) Prior systemic therapy Prior radiation therapy Prior surgery 43 (61) 16 (23) 31 (44) 44 (61) 16 (22) 44 (61) Patients with uncontrolled pain per BPI - SF API >4, n (%) b 16 (23) 14 (19) Kasper et al. DeFi Phase 3 in Adult Desmoid Tumors

Content of this presentation is copyright and responsibility of the author. Permission is required for re - use . Nirogacestat Significantly Reduced Risk of Disease Progression Median follow - up time was 19.2 months for nirogacestat and 10.9 months for placebo. NE, not estimable. No. of Patients No. of Events Median (95% CI) Hazard ratio (95% CI) Nirogacestat 70 12 NE (NE, NE) P <0.001 0.29 (0.15, 0.55) Placebo 72 37 15.1 (8.4, NE) Kasper et al. DeFi Phase 3 in Adult Desmoid Tumors

Content of this presentation is copyright and responsibility of the author. Permission is required for re - use . PFS Benefit With Nirogacestat Was Observed Across Prespecified Subgroups PFS, progression - free survival; TKI, tyrosine kinase inhibitor. Kasper et al. DeFi Phase 3 in Adult Desmoid Tumors Favors placebo Favors nirogacestat Hazard Ratio Nirogacestat Censored/Events Placebo Censored/Events Sex Male 0.26 21 / 4 14 / 11 Female 0.30 37 / 8 21 / 26 APC mutation Yes 0.20 9 / 2 3 / 8 CTNNB1 mutation Yes 0.28 37 / 6 21 / 21 Target tumor location Intra - abdominal 0.17 15 / 2 7 / 11 Extra - abdominal 0.34 43 / 10 28 / 26 Focality Single 0.29 37 / 6 22 / 19 Multifocal 0.30 21 / 6 13 / 18 Prior surgery Yes 0.31 26 / 5 21 / 23 No 0.33 32 / 7 14 / 14 Prior chemotherapy Yes 0.24 19 / 5 10 / 17 No 0.32 39 / 7 25 / 20 Prior TKI treatment Yes 0.15 19 / 4 8 / 16 No 0.38 39 / 8 27 / 21 0.00 1.00 2.00 Hazard Ratio (95% CI) Nirogacestat vs Placebo

Content of this presentation is copyright and responsibility of the author. Permission is required for re - use . Objective Response Rate by Blinded Independent Central Review a Duration of objective response was defined as duration in months from the time CR or PR (which ever came first) was met until th e date of progression, death, or censoring. CR, complete response; NE, not estimable; PR, partial response. Nirogacestat (n=70) Placebo (n=72) Objective response rate (CR+PR), n (%) 95% CI Two - sided P value 29 (41) (30.2, 54.5) <0.001 6 (8) (3.1, 17.3) Best overall response, n (%) Complete response Partial response Stable disease Progressive disease Not evaluable 5 (7) 24 (34) 35 (50) 1 (1) 4 (6) 0 6 (8) 55 (76) 10 (14) 1 (1) Time to objective response, median (range), mo 5.6 (2.6, 19.4) 11.1 (2.8, 16.4) Kaplan - Meier estimate of median duration of objective response (95% CI), mo a NE (NE, NE) NE (8.3, NE) Kasper et al. DeFi Phase 3 in Adult Desmoid Tumors

Content of this presentation is copyright and responsibility of the author. Permission is required for re - use . Placebo * Nirogacestat Nirogacestat Treatment Resulted in Substantial Reductions in Tumor Size Change in tumor size, % *Patient had a complete resolution of the target lesion but still had documented non - target lesion; therefore, not a complete re sponse. Best percent change values are averaged between 2 blinded independent reviewers unless a reader was selected for adjudication , i n which case only the adjudicated value is presented. Kasper et al. DeFi Phase 3 in Adult Desmoid Tumors *

Content of this presentation is copyright and responsibility of the author. Permission is required for re - use . Nirogacestat Significantly Reduced Pain Severity Compared With Placebo Mean (SD ) baseline scores: nirogacestat, 3.2 (3.26 ) ; placebo, 3.3 (3.31 ). Differences at Cycle 10 were statistically significant and clinically meaningful. LS mean change from baseline represents the 7 - day average. LS, least squares. Brief Pain Inventory - Short Form – Average Pain Intensity LS mean (SE) Nirogacestat Placebo Difference Cycle 10 −1.5 (0.3) −0.04 (0.3) −1.5 P <0.001 Kasper et al. DeFi Phase 3 in Adult Desmoid Tumors Worsening Improvement

Content of this presentation is copyright and responsibility of the author. Permission is required for re - use . Nirogacestat Significantly Reduced DT - Specific Symptom Severity Mean (SD) baseline scores: nirogacestat, 3.4 (2.34); placebo, 3.5 (2.57). Differences at Cycle 10 were statistically signific ant and clinically meaningful. DTSS total symptom score includes pain, fatigue, swelling, muscle weakness, and difficulty moving. DT, desmoid tumor; DTSS, GODDESS DT Symptom Scale; GODDESS, GOunder/Desmoid Tumor Research Foundation DEsmoid Symptom/Impact Sca le; LS, least squares. GODDESS DTSS – Total Symptom Score Kasper et al. DeFi Phase 3 in Adult Desmoid Tumors LS mean (SE) Nirogacestat Placebo Difference Cycle 10 −1.2 (0.2) 0.4 (0.2) −1.6 P <0.001 Worsening Improvement

Content of this presentation is copyright and responsibility of the author. Permission is required for re - use . Nirogacestat Significantly Improved Physical/Role Functioning and QoL Mean (SD) baseline scores: nirogacestat, 2.8 (1.14); placebo, 2.7 (1.24). Differences at Cycle 10 were statistically signific ant and clinically meaningful. DTIS physical functioning includes moving, reaching, vigorous activity, moderate activity, accompl is hing less. DT, desmoid tumor; DTIS, GODDESS DT Impact Scale; EORTC QLQ - C30, European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire - Core 30; GODDESS, GOunder /Desmoid Tumor Research Foundation DEsmoid Symptom/Impact Scale; LS, least squares; QoL, quality of life. Kasper et al. DeFi Phase 3 in Adult Desmoid Tumors ▪ Nirogacestat also significantly improved EORTC QLQ - C30 physical functioning ( P <0.001), role functioning ( P <0.001), and global health status/QoL ( P= 0.007) at Cycle 10 compared with placebo Worsening Improvement LS mean (SE) Nirogacestat Placebo Difference Cycle 10 −0.7 (0.1) 0.2 (0.1) −0.8 P <0.001 GODDESS DTIS – Physical Functioning Impact Score

Content of this presentation is copyright and responsibility of the author. Permission is required for re - use . Nirogacestat Safety Profile a Death due to sepsis. b TEAEs leading to discontinuations in ≥1 patient include gastrointestinal disorders (n=5 [4%]), ovarian dysfunction (n=4 [3%]) , a lanine aminotransferase increase (n=3 [2%]), aspartate aminotransferase increase (n=2 [1%]), and metabolism/nutritional disorders (n=2 [1%]). TEAE, treatment - emergent adverse event. Safety population, n (%) Nirogacestat (n=69) Placebo (n=72) Duration of study drug exposure, median (range), months 20.6 (0.3, 33.6) 11.4 (0.2, 32.5) Dose intensity, median (range), mg/d 288.3 (169, 300) 300.0 (239, 300) Any Grade Grade ≥3 Any Grade Grade ≥3 Any TEAE 69 (100) 39 (57) 69 (96) 12 (16) TEAEs of any grade reported in ≥25% of patients in either arm Diarrhea 58 (84) 11 (16) 25 (35) 1 (1) Nausea 37 (54) 1 (1) 28 (39) 0 Fatigue 35 (51) 2 (3) 26 (36) 0 Hypophosphatemia 29 (42) 2 (3) 5 (7) 0 Rash, maculopapular 22 (32) 4 (6) 4 (6) 0 Headache 20 (29) 0 11 (15) 0 Stomatitis 20 (29) 3 (4) 3 (4) 0 TEAEs leading to death 0 1 (1) a Dose reductions due to TEAEs 29 (42) 0 Discontinuations due to TEAEs 14 (20) b 1 (1) b Kasper et al. DeFi Phase 3 in Adult Desmoid Tumors ▪ 95% of TEAEs were Grade 1 or 2; the first onset of TEAEs in most patients occurred during Cycle 1

Content of this presentation is copyright and responsibility of the author. Permission is required for re - use . Frequency and Resolution of Ovarian Dysfunction Observed With Nirogacestat a OD among women of childbearing potential was defined by investigators who reported the MedDRA Preferred Terms of amenorrhea, premature menopause, menopause, and ovarian failure. b As of July 20, 2022. c Resolution of OD events was defined by the investigator. OD, ovarian dysfunction. 1. Thurston et al. Obstet Gynecol Clin North Am. 2011;38:489 - 501. 2. Mauri et al. Front Endocrinol (Lausanne). 2020;11:572388. 27 of 36 women of childbearing potential reported OD (75%) 11 patients discontinued nirogacestat for any reason (41%) OD resolved b in 11 patients (100%) 14 patients ongoing nirogacestat treatment (52%) OD resolved b in 9 patients (64%) Unresolved OD in 5 patients (36%) 2 patients lost to follow - up after discontinuing nirogacestat (7%) OD status unknown Kasper et al. DeFi Phase 3 in Adult Desmoid Tumors ▪ OD is a composite adverse event associated with changes in female reproductive hormone levels and clinical manifestations 1,2 ▪ Protocol - mandated serum hormone collection at baseline and cycles 1, 2, 4, and every 3 thereafter ▪ Among women of childbearing potential, OD a was observed in 75% receiving nirogacestat and 0% receiving placebo – Median time to first onset of OD: 8.9 weeks – Median duration of OD events: 21.3 weeks

Content of this presentation is copyright and responsibility of the author. Permission is required for re - use . ▪ DeFi represents the largest and most rigorous randomized controlled trial conducted to date in DT – DeFi is also the first Phase 3, randomized, controlled trial to demonstrate clinical benefit with a GSI in any indication ▪ Nirogacestat demonstrated rapid, sustained, and statistically significant improvements in all primary and secondary efficacy endpoints – 71% reduction in the risk of disease progression as compared with placebo – Objective response rate of 41%, including a 7% complete response rate – Statistically significant and clinically meaningful improvements in pain, disease - specific symptom burden, physical/role functio ning, and overall quality of life ( P ≤0.007 ) ▪ Nirogacestat exhibited a manageable safety profile, with 95% of all treatment - emergent adverse events being Grade 1 or 2 ▪ Nirogacestat has the potential to become the standard of care for patients with DT requiring systemic treatment Summary Kasper et al. DeFi Phase 3 in Adult Desmoid Tumors DT, desmoid tumor, GSI, gamma secretase inhibitor.

Content of this presentation is copyright and responsibility of the author. Permission is required for re - use . Acknowledgments ▪ We thank the DeFi trial participants, their families, and trial personnel ​ ▪ We thank these DeFi Principal Investigators for their contributions to participant enrollment and data acquisition: Charlotte Benson, Nam Quoc Bui, Rashmi Chugh, Gabriel Tinoco, John Charlson, Palma Dileo, Lee Hartner, Lore Lapeire, Filomena Mazzeo, Emanuela Palmerini, Peter Reichardt, Silvia Stacchiotti, Howard H. Bailey, Melissa A. Burgess, Gregory M. Cote, Lara E. Davis, Hari Deshpande, Hans Gelderblom, Giovanni Grignani, Elizabeth Loggers, Tony Philip, Joseph G. Pressey ​ ▪ We thank the former DeFi Principal Investigators for their contributions: Victor Villalobos, Jonathan Trent, Robert Maki, Suzanne George, Michael Nathenson , and Amanda Parkes; and the DeFi Principal Investigators who contributed to the screening of trial participants: Christian Meyer, Mark Agulnik , James Hu, Vicki Keedy, and Jade Homsi ​ ▪ We thank the data monitoring committee members: Timothy Cripe, Damon Reed, Stephen Skapek , and Barry Turnbull ​ • We thank The Desmoid Tumor Research Foundation and Sarcoma Patients Advocacy Global Network (SPAGN) ▪ Medical writing and editorial support was provided by MedThink SciCom ▪ DeFi was sponsored by SpringWorks Therapeutics, Inc. BK : University of Heidelberg, Mannheim University Medical Center, Mannheim Cancer Center, Sarcoma Unit, Mannheim, Germany. RR : MD Anderson Cancer Center, Houston, TX, USA. TA : McGill University Health Center, Montreal, Quebec. PS : University Hospitals Leuven, Leuven, Belgium. WTG : Netherlands Cancer Institute, Amsterdam, The Netherlands. RFR : University of Colorado Anschutz Medical Campus, Aurora, CO, USA; Duke Cancer Institute, Durham, NC, USA. AL, LMS : SpringWorks Therapeutics, Stamford, CT, USA. SM : PharPoint Research, Durham, NC, USA. SA : Mayo Clinic, Jacksonville, FL, USA. SC : Sarcoma Oncology Center, Santa Monica, CA, USA. GD : University of Miami Sylvester Cancer Center, Miami, FL, USA. NF : David Geffen School of Medicine, University of California, Los Angeles, CA, USA; UCLA Jonsson Comprehensive Cancer Center, Los Angeles, CA, USA. PM : Dana - Farber Cancer Institute, Boston, MA, USA. BAVT : Washington University, St. Louis, St Louis, MO, USA. BV: Policlinico Universitario Campus Bio - Medico, Rome, Italy. SK : Division of Hematology & Medical Oncology, Oregon Health & Science University, Portland, OR, USA. MG : Memorial Sloan Kettering Cancer Center, Weill Cornell Medical College, New York City, NY, USA. Kasper et al. DeFi Phase 3 in Adult Desmoid Tumors Author Affiliations For questions or to request a copy of this presentation, please contact SpringWorks Medical Information at: Email: medinfo@springworkstx.com Web: SpringWorks (springworkstxmedical.com) Dr. Kasper’s Email: bernd.kasper @umm. de Correspondence

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